Introduction. Сommunity-acquired pneumonia (COP) is a global socio-medical problem. At emergence of pneumonia by any genesis, hypoxia develops. Oxygen homeostasis of the body is provided by the coordinated interaction of external respiration, circulatory system and oxygen-transport system of the blood. Hypoxia, due to the malfunction of the external respiratory system, causes the formation of compensatory changes, in the implementation of which involved components of the oxygen transport system. Molecular genetic mechanisms play an important role in the body's adaptation to oxygen deficiency. Fetal hemoglobin (FetHb), having an increased affinity for oxygen, makes a significant contribution to the body's adaptation to new conditions with altered gaseous environment in the presence of pathological processes occurring with hypoxia. In this regard, it is interest to determine FetHb in adults with COP to study its effect on the diagnosis, prognosis and outcome of the disease. The aim of the study. To determinate the participation of the organism adaptation mechanisms to the lack of oxygen according to the assessment of the content of fetal hemoglobin in the peripheral blood of patients with community-acquired pneumonia. Materials and methods. We examined 34 adult patients (18 women and 16 men) with COP, aged 18 to 80 years, who were in the therapeutic department of the City Clinical Hospital № 25 in Kharkiv. The control group was formed of 20 healthy individuals. Spirography was performed on the diagnostic complex "Valenta"; hematological examinations – on the analyzer "ADVIA 60"; measurement of pO2 and pCO2, oxygen saturation, content of fetal hemoglobin – on the device "RAPIDLAB865". Results. In patients with community-acquired pneumonia, there was a decrease of the ventilatory function of external respiration, which is confirmed by a marked decrease in partial oxygen pressure. Oxygen saturation of blood was reduced in the group of patients with COP, but the difference was not statistically significant 94.8 ± 1.0 %. This indicates the presence of compensatory mechanisms aimed at maintaining adequate blood oxygen saturation. Significant increase in pH (from 7.40 to 7.53) and decrease in standard bicarbonate (from 1.27 to 0.68 mmol/l) resulting from violation of the gas composition of the blood can be regarded as a manifestation of partially compensated respiratory alkalosis. In patients with COP, there was a reduction in the total time of hemolysis, a shift of the maximum erythrogram to the left and an increase in the maximum itself, indicating a sharp decline in erythrocyte resistance. The proportion of erythrocytes with reduced resistance was twice as large as similar forms in the control group and the number of highly resistant cells in patients with COP sharply decreased. Obviously, oxygen starvation-mediated stress erythropoiesis is accompanied by the entry into the circulation of functionally defective erythrocytes. They are subject to accelerated elimination from the vascular bed, which causes a decrease in the quantitative indicators of red blood (erythrocyte content, hemoglobin) while maintaining corpuscular parameters (Mean Corpuscular Volume, Mean Cell Hemoglobin Concentration). At the same time, the analysis of individual hemoglobin fractions revealed an increase in the proportion of fetal hemoglobin (from 2.90 ± 0.31 % in the group of healthy individuals to 5.43 ± 1.05 % in patients with COP) (p less than 0.05). Conclusions. Changes in the parameters of acid hemolysis, fetal hemoglobin in the peripheral blood of patients with community-acquired pneumonia with impaired pulmonary ventilation function indicate their participation in the mechanisms of adaptation to oxygen deficiency and they have informative potential. Elevated fetal hemoglobin in peripheral blood in these patients can be used as an indicator of hypoxia, accompanied by impaired oxygen delivery to tissues, which should be used as an additional criterion for diagnosing tissue hypoxia and justify the timely appointment of antihypoxia drugs. Keywords: hypoxia, community-acquired pneumonia, red blood cells, fetal hemoglobin.
Structure of pulmonary non-elastic resistance in community-acquired pneumonia
